4.7 Article

The effects of puberty on genetic risk for disordered eating: evidence for a sex difference

期刊

PSYCHOLOGICAL MEDICINE
卷 42, 期 3, 页码 627-637

出版社

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291711001541

关键词

Eating disorders; genetics; males; puberty; sex differences; twins

资金

  1. National Institute of Mental Health (NIMH) [1R01 MH092377-01, 1R21 MH070542-01, 1F31-MH084470]
  2. Michigan State University

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Background. Differences in genetic influences on disordered eating are present across puberty in girls. Heritability is 0% before puberty, but over 50% during and after puberty. Emerging data suggest that these developmental differences may be due to pubertal increases in ovarian hormones. However, a critical piece of evidence is lacking, namely, knowledge of genetic influences on disordered eating across puberty in boys. Boys do not experience increases in ovarian hormones during puberty. Thus, if pubertal increases in genetic effects are present in boys, then factors in addition to ovarian hormones may drive increases in heritability in girls. The current study was the first to examine this possibility in a sample of 1006 male and female twins from the Michigan State University Twin Registry. Method. Disordered eating was assessed with the Minnesota Eating Behavior Survey. Pubertal development was assessed with the Pubertal Development Scale. Results. No significant differences in genetic influences on disordered eating were observed in males across any developmental stage. Heritability was 51% in boys during pre-puberty, puberty and young adulthood. By contrast, in girls, genetic factors accounted for 0% of the variance in pre-puberty, but 51% of the variance during puberty and beyond. Sex differences in genetic effects were only significant during pre-puberty, as the best-fitting models constrained heritability to be equal across all males, pubertal females and young adult females. Conclusions. The results highlight sex-specific effects of puberty on genetic risk for disordered eating and provide indirect evidence of a role for ovarian hormones and/or other female-specific factors.

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